Application Of Footshock Research Articles

Noradrenergic influences in the basolateral amygdala on inhibitory avoidance memory are mediated by an action on α2-adrenoceptors.

The role of norepinephrine (NE) in the consolidation of inhibitory avoidance learning (IA) in rats is known to involve α1- and β-adrenoceptor systems in the basolateral nucleus of the amygdala (BLA). However, the amygdala also contains α2-adrenoceptor subtypes, and local microinfusions of the selective α2-adrenoceptor antagonist idazoxan and agonist UK 14,304 respectively into the BLA enhance and inhibit IA performances when administered before acquisition. The present study investigated whether the effects of idazoxan and UK 14,304 on IA were associated with changes in NE release within the BLA before and after one-trial inhibitory avoidance training. Male Sprague-Dawley rats were unilaterally implanted with a microdialysis probe in the BLA and were administered idazoxan (0.1mM) or UK 14,304 (10 μM) by retrodialysis infusion 15 min before the acquisition of IA. Dialysates were collected every 15 min for analysis of NE. Retrodialysis of idazoxan potentiated the release of NE induced by footshock application, whereas UK 14,304 decreased NE release to the extent that the footshock failed to induce any measurable effect on NE levels. Idazoxan infusion enhanced IA retention tested 24h later and this effect was directly related to the level of NE release in the BLA measured during IA acquisition. In contrast, the infusion of UK 14,304 did not modify IA performances in comparison to control animals, possibly due to compensatory activity of the contralateral BLA. These results are consistent with previous evidence that amygdala NE is involved in modulating memory consolidation, and provide evidence for an involvement of presynaptic α2-autoceptors in the BLA in this process.

Aversive and non-reward learning in the fire-bellied toad using familiar and unfamiliar prey stimuli

Abstract The present study investigated how snapping behavior toward familiar and unfamiliar prey is modified by reward omission and aversive conditioning in the fire-bellied toad Bombina orientalis. Toads were trained to snap at cricket images by rewarding them with live crickets. The task was learned, and the learning criterion (10 snapping responses within 2 minutes) was reached in all individuals investigated. Subsequent reward omission did not alter the frequency of snapping to the familiar cricket stimulus. Snapping decreased only in some individuals, when a mild foot shock was applied at snapping. However, at presentation of images of hitherto unfamiliar meal worms and foot-shock application at snapping to the stimulus, the majority of toads diminished snapping significantly. Snapping responses decreased more rapidly, when snapping at meal worms was not rewarded or a footshock was applied uncorrelated to the presentation of or snapping at meal worms. These results demonstrate that in toads familiarity and unfamiliarity of prey stimuli are important factors in aversive learning, because well-trained responses to familiar stimuli become immune against reward omission. Furthermore, at presentation of unfamiliar stimuli, omission of reward and uncorrelated footshock had a stronger aversive effect than correlated footshock.

Changes in β-Endorphin-Like-lmmunoreactivity in the Blood Plasma of Ewes during Estrous Cycle and in Anestrous Ewes under Stress Condition

In the light of evidence for endogenous opioid peptide involvement in the modulation of pituitary hormone release and in the body's overall response to stress, the aim of the present study was to determine the beta-endorphin-like immunoreactivity (beta-END-LI) in the blood plasma of ewes during different phases of the estrous cycle and in anestrous ewes subjected to acute or intermittent prolonged footshocks. The highest concentration of beta-END-LI was found in the blood plasma during the luteal phase and lowest one during the follicular stage at proestrus. Nearly equal concentrations of beta-END-LI were determined at estrus and metestrus; their values were over 10 times lower than those observed in the luteal phase. Acute stress caused transient increase of beta-END-LI in the blood plasma of anestrous ewes, with a peak after 15-30 min of footshock application and changes in the molar ratio of beta-LPH to beta-endorphin. No apparent increase in mean daily levels of beta-END-LI was noted in ewes subjected to prolonged footshocking; however, on the day after stimulation beta-END-LI concentration decreased below control values. These results indicate that: 1. secretion of beta-END-LI varies during different phases of the estrous cycle, 2. acute stress is a potent activator for beta-END-LI secretion, 3. no apparent increase of beta-END-LI in the blood plasma of ewes subjected to prolonged stress concomitant with accumulation of this material in pituitary (Polkowska and Przekop, 1988) supports the idea, that prolonged stress augments the synthesis of beta-END-LI but not its release.

Differences in the behaviour of Sprague–Dawley and Lewis rats during repeated passive avoidance procedure: effect of amphetamine

The present paper investigated the differences in passive avoidance learning between Sprague–Dawley and Lewis rats. After initial habituation (experimental Part 1), measured as latencies to enter the dark, preferable compartment, the effect of treatment with amphetamine (8 mg kg−1b.w.), the retention performance compared with controls (saline) was tested in both rat strains in Parts 2–4 . The intervals between Parts 2–4 were 24 or 49 days. Each experimental part consisted of testing lasting 6 days. On the 7th day the rats received drug treatment 1 h before the application of foot shock. The differences between rat strains were already detectable at the beginning of the study. During the repeated exposures of rats in Part 1, only Lewis rats, in contrast to Sprague–Dawley rats, exhibited the habituation. The repeated testing of rats in Parts 2–4, due to previous experience with an aversive stimulus, was considered as the retention test. In Parts 2–3 we observed only minor differences in the responses of both rat strains tested. Also no significant differences were observed between rat strains after amphetamine treatment that induced an amnesia-like effect in all retention trials. However, data shown in Part 4 revealed the largest differences between both strains. Control Lewis rats exhibited significantly higher retention responses than Sprague–Dawley rats. In the latter strain we observed no differences in avoidance latencies between controls and amphetamine treated rats. In Lewis rats the difference in avoidance performance between controls and amphetamine treated animals was highly significant due to their enhanced retention performance. In conclusion, the results presented in this study extend the known behavioural differences in tested rat strains to the passive avoidance procedure that, in addition, was performed for a total period of 4 months. Due to a known deficiency of hypothalamo-pituitary-adrenal axis activity in Lewis rats it can be hypothesized that the behavioural dissociation of this strain from Sprague–Dawley rats could be related to the different activity of this regulatory axis in the rat strains tested.

The effects of early postnatal stimulation on Morris water-maze acquisition in adult mice: genetic and maternal factors.

Following stressor exposure BALB/cByJ mice exhibit hypersecretion of corticosterone and marked brain catecholamine alterations. In addition, mice of this strain exhibit impairments of performance in a Morris water-maze, which may be exacerbated by footshock application. In the present investigation it was demonstrated that early-life handling of mouse pups (coupled with brief separation periods from the dam over the course of 21 days postpartum) reduced the learning impairments seen when mice were tested in the Morris water-maze at 120 days of age and also prevented stress-induced disturbances in this task. Likewise, cross-fostering BALB/cByJ mice with a C57BL/6ByJ dam prevented the performance deficits. In contrast, C57BL/6ByJ mice cross-fostered to a BALB/cByJ dam exhibited proficient performance. Thus, maternal factors may be important in determining the Morris water-maze disturbances, provided that this was applied on the BALB/cByJ genetic background. Stressor exposure exacerbated the performance disturbances in BALB/cByJ mice, while diazepam treatment disrupted Morris water-maze performance in both BALB/cByJ and C57BL/6ByJ mice. Paralleling the behavioral changes associated with handling, the stress-induced hypercorticosterone secretion characteristic of the BALB/cByJ mouse was attenuated by the early handling procedure. Stressor exposure also produced strain-dependent variations of NE and 5-HT, but these effects were not appreciably influenced by the handling procedure. These data are consistent with the proposition that performance disturbances of BALB/cByJ mice tested in the Morris water-maze task are associated with excessive hypothalamic-pituitary-adrenal reactivity. Moreover, it appears that the influence of early-life stimulation may interact with genetic factors in determining endocrine and behavioral stress responses.

Stress and/or tranylcypromine treatment affects serotonergic measures in blood and brain in rats

Since stress can alter serotonin (5-hydroxytryptamine, 5-HT) turnover in the brain and the periphery, the effects of different types of acute stress on serotonin and related substances in the whole blood and various brain areas in rats pretreated with tranylcypromine (TCP) were studied. TCP administered alone caused a rise in 5-HT, a fall in its metabolite (5-hydroxyindoleacetic acid, 5-HIAA) in the whole blood and in every part of the brain analyzed relative to controls. In rats given TCP and subjected to footshock or water-immersion restraint stress similar changes, but to a different extent, were observed. 5-HT level remained essentially constant except in the blood and the limbic system, whereas 5-HIAA level was found to be increased in the blood and the brain, mainly in the limbic system and the brainstem following footshock. Water-immersion restraint stress caused an increase in 5-HT only in the limbic system without any changes in 5-HT and 5-HIAA in the blood. Relative to controls, an increase in total tryptophan concentration in the whole blood and in every part of the brain was found only after footshock application with or without pretreatment with TCP. In conclusion, responses to stress in rats may depend upon the type of stimulus applied as well as of a concurrent administration of TCP. Some regional differences may account for an altered in vivo efficacy of this drug.

Stress-dependent changes in fibrinolysis, serotonin and platelet aggregation in rats

The effects of different kinds of acute stress on collagen-induced whole blood platelet aggregation and fibrinolysis in relation to blood serotonergic measures were studied. In rats water-immersion restraint stress resulted in a shortening of euglobulin clot lysis time (ECLT), an increase in tissue plasminogen activator(tPA) activity with a concurrent fall in its inhibitor activity. Footshock caused rather a suppression in fibrinolysis with a prolongation of ECLT and a decline in tPA activity as well as a reduction in whole blood platelet aggregation induced by collagen. Serotonin (5-HT) level, a marker of a severity of stress, increased after footshock application with a concomitant rise in its major metabolite-5-hydroxyindoleacetic acid (5-HIAA). This indicates an enhanced 5-HT metabolism. Following water-immersion restraint stress 5-HT and 5-HIAA levels did not differ from controls. In both groups of stressed animals an inverse correlation between tPA activity and blood serotonin was observed. Our data indicate that these types of stress may influence either fibrinolysis or peripheral serotonergic mechanism in different ways. Acute and severe stress such as footshock by causing an impairment in fibriinolysis and a rise in 5-HT may contribute to the pathogenesis of thrombosis and henceforth to the development of atherosclerosis.

Ontogeny of Stress-Induced Ultrasonic Vocalization and Pituitary-Adrenal Hormone Secretion in Preweanling Norway Rats

Adult organisms rapidly exhibit protective behavioral responses when threatened. In addition, physiological systems are activated reflexively to facilitate survival. How these defensive systems are integrated in order to produce appropriate responding demands a developmental psychobiological analysis. This paper summarizes studies examining in the Norway rat the concurrent ontogeny of 30-50 kHz ultrasonic vocalizations and pituitary-adrenal hormone responses induced by stressors presented during the preweaning period. Postnatal Day 7 male rats exposed to social isolation emit significantly more ultrasounds than Day 14 pups, and by 21 days of age social isolation is no longer effective in eliciting ultrasonic vocalizations. This age-dependent attenuation in occurrence of ultrasounds is accompanied by an increased responsiveness of the pituitary- adrenal system. Studies incorporating the use of psychophysical, that is, electric foot shock, and psychological, that is, conspecific threat, stressors indicate further that exposure to such stimuli significantly reduces in Day 14 rats the emission of ultrasonic vocalization but may potentiate their occurrence in Day 7 pups. Application of foot shock reliably induces ultrasonic emission in normally silent Day 21 pups as in adult rats. The hormonal response to these stressors is similar to that found in pups exposed to social isolation; pituitary adrenocorticotropin and adrenal corticosterone secretion increases significantly in Day 14 pups and a further notable increased secretion occurs in Day 21 males and reflects the intensity of the stressor. The increased secretion of pituitary-adrenal hormones coupled with the modulatory capacity to reduce ultrasonic vocalizations by 14 days of age suggest that systems have developed to provide increased behavioral and physiological flexibility during confrontations with varied threats.

Blockade of the Development of Analgesic Tolerance to Morphine by Concurrent Treatment with Opioid- But Not Non-Opioid-Mediated Stress in Mice

Studies have been carried out to determine how the analgesic effect of morphine and the development of tolerance to the effect would be influenced by concurrent exposure to stresses in mice. Application of footshock (FS) stress, which produces analgesia mediated by opioid μ-receptors, or psychological (PSY) stress, which produces analgesia in a manner more closely related to opioid κ-receptors, did not affect the analgesic effect of morphine, but completely blocked the development of tolerance during 5 daily concomitant treatments. On the other hand, forced swimming (SW) stress induced analgesia (SIA), which was not antagonized by naloxone, suppressed morphine analgesia, but failed to block the tolerance development. The blockade of the development of tolerance to morphine analgesia by stresses may not be attributed to the analgesic effect induced by the stresses because a combination of weak FS stress, which induces no analgesia, also effectively suppressed the development of morphine tolerance. In addition to the opioid mechanism, an adrenergic mechanism can not be excluded because of the reserpine antagonism of these SIAs.

Blockade of the development of analgesic tolerance to morphine by concurrent treatment with opioid- but not non-opioid-mediated stress in mice.

Studies have been carried out to determine how the analgesic effect of morphine and the development of tolerance to the effect would be influenced by concurrent exposure to stresses in mice. Application of footshock (FS) stress, which produces analgesia mediated by opioid mu-receptors, or psychological (PSY) stress, which produces analgesia in a manner more closely related to opioid kappa-receptors, did not affect the analgesic effect of morphine, but completely blocked the development of tolerance during 5 daily concomitant treatments. On the other hand, forced swimming (SW) stress induced analgesia (SIA), which was not antagonized by naloxone, suppressed morphine analgesia, but failed to block the tolerance development. The blockade of the development of tolerance to morphine analgesia by stresses may not be attributed to the analgesic effect induced by the stresses because a combination of weak FS stress, which induces no analgesia, also effectively suppressed the development of morphine tolerance. In addition to the opioid mechanism, an adrenergic mechanism can not be excluded because of the reserpine antagonism of these SIAs.

Increased shock induced aggression during morphine withdrawal

Spontaneous fighting and footshock-induced aggression of male Wistar rats were recorded before and during morphine administration to produce dependence, and after withdrawal. The morphine dependent rats showed spontaneous fighting on the 3rd through 5th days of withdrawal. However, application of footshock during morphine withdrawal enabled the detection of increased aggressiveness from the 2nd day through the 12th day after the last injection of morphine. This method thus detected a considerably more protracted enhancement of aggression by withdrawal than has been reported previously. In this way it proved superior to simply recording spontaneous aggression, and at the same time it gave a reduced variability compared to the high level seen with measures of spontaneous aggression.